Abstract

Acute myeloid leukemia is obviously a heterogeneous disease, different entities being distinguishable by differences in morphology, karyotype, disturbances in the expression of proto-oncogenes, clinical course etc. Some five years ago we made observations that indicated that one mechanism of leukemogenesis involved the malignant cell beginning to produce a hemopoietic growth factor that stimulated its own growth (Schrader and Crapper, 1983). Experiments in which cell-lines have been rendered leukemogenic by infection with retroviruses encoding hemopoietic growth factor genes, have formally confirmed the hypothesis that the inappropriate production of an autostimulatory growth factor by a hemopoietic cell that was immortal but not leukemogenic, could convert the cell to a transplantable leukemia (Lang, et al., 1985; Campbell, et al., 1987 and Nienhuis et al., this volume). Here, we summarize experiments that suggest that perturbations of growth factor production may be a relatively frequent feature of the leukemogenic process and that genetic techniques may allow pinpointing of diseases that involve this mechanism.